Crohn’s Disease, Obesity Clinical Trial
Official title:
Crohn’s Disease, Obesity and Disease Severity
The aim of our study is to suggest possible underlying mechanisms for the observed clinical differences in disease severity and behavior of overweight and obese patients with crohn's disease(BMI > 25 kg/m²)as compare to non-obese crohn's patients with a normal or low weight ( BMI ≤ 25) by measuring metabolic\nutritional variables and cytokine levels.
Crohn’s disease (CD) is a chronic intestinal disorder of unknown etiology that may involve
any part of the gastrointestinal tract. The small bowel is involved in 70% of CD patients.
Undernutrition expressed in low body mass index (BMI) <18.5 kg/m², is a common presentation
and has been reported in 65–75% of these patients. Possible pathogenic mechanisms include
inadequate dietary intake ,increased energy expenditure, nutrient malabsorption and
intestinal losses. We have studied recently these three important components of energy
balance of underweight crohn’s patients and found that nutrient malabsorption may play a
role.
Although the majority of crohn's disease patients are undernourished , some of them are
surprisingly obese and their symptoms seem be more severe; Blain A et al. have reported
recently that obesity in CD has been associated with more frequent anoperineal complications
and a more marked disease activity. Hass J et al have found that overweight CD patients
require earlier surgical intervention and perhaps more aggressive medical therapy.
Notwithstanding, the characteristics of CD and possible underlying pathophysiological
mechanisms in obese patients have not been studied yet.
Mesenteric hypertrophied fat commonly called “creeping fat is a common feature of crohn's
disease and has been reported to correlate with ulceration, stricture formation and
transmural inflammation. It is a matter of debate whether the development of creeping fat is
a causative or secondary phenomenon ,but there is increasing body of evidence that suggest
that mesenteric adipose tissue plays an active role in the pathogenesis of creeping fat and
mesenteric inflammation by pro-inflammatory and anti-inflammatory adipocytokines.
Recently there is more recognition that adipose tissue is not a passive connective tissue
merely storing fat but an activeendocrine organ which participates in numerous physiological
and pathophysiological processes with variety of secretory products designated
adipocytokines that regulate metabolic processes in an endocrine ,paracrine and autocrine
manner Moreover, Obesity is increasingly being recognized as a risk factor for a number of
gastrointestinal conditions as well as being characterized by a chronic, systemic low-grade
state of inflammation per se. Biomarkers of inflammation, such as the leukocyte count, tumor
necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), and C-reactive protein, are
increased in obesity and have been related to insulin resistance and the metabolic syndrome.
;
Observational Model: Defined Population, Time Perspective: Cross-Sectional